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Alteration of gut microbial ecology by the direct activation of the brain: Inverse gut-microbiome-brain dynamics.
The gut-microbiome-brain axis is a bidirectional communication system influencing host physiology and overall fitness. While "bottom-up" effects-where gut microbes influence brain function and behavior-are well established, direct evidence for "top-down" modulation-where the brain shapes the gut microbial ecology-remains elusive. Here, we show that the selective expression of the bacterial ion channel mNaChBac in glutamatergic lateral habenula (LHb) neurons increases their bursting activity and leads to endophentypes associated with depression. Importantly, this chronic activation leads to changes in the gut microbiome composition over time, as reflected by shifts in alpha-diversity and alterations in specific microbial taxa. These findings provide direct evidence that the persistent activation of the brain acts as a selective pressure that affects the stability and diversity of the gut microbiome, providing a new dimension by which gut-microbiome-brain interactions may cooperate to modulate host physiology and health.
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Association of maternal postpartum depression symptoms with infant neurodevelopment and gut microbiota.
INTRODUCTION: Understanding the mechanisms underlying maternal postpartum depression (PPD) and its effects on offspring development is crucial. However, research on the association between maternal PPD, gut microbiota, and offspring neurodevelopment remains limited. This study aimed to examine the association of maternal PPD symptoms with early gut microbiome, gut metabolome, and neurodevelopment in infants at 6 months. METHODS: Maternal PPD symptoms were assessed using the Edinburgh Postpartum Depression Scale (EPDS) at 42 days postpartum. Infants stool samples collected at 42 days after birth were analyzed using 16S rRNA sequencing and liquid chromatography-mass spectrometry (LC-MS) detection. Infant neurodevelopment was measured at 6 months using the Ages and Stages Questionnaire, Third Edition (ASQ-3). Correlations between gut microbiota, metabolites and neurodevelopment were identified through co-occurrence network analysis. Finally, mediation analyses were conducted to determine potential causal pathways. RESULTS: A total of 101 mother-infant dyads were included in the final analysis. Infants born to mothers with PPD symptoms at 42 days postpartum had lower neurodevelopmental scores at 6 months. These infants also had increased alpha diversity of gut microbiota and were abundant in Veillonella and Finegoldia, while depleted abundance of Bifidobacterium, Dialister, Cronobacter and Megasphaera. Furthermore, alterations were observed in metabolite levels linked to the Alanine, aspartate, and glutamate metabolic pathway, primarily characterized by decreases in N-Acetyl-L-aspartic acid, L-Aspartic acid, and L-Asparagine. Co-occurrence network and mediation analyses revealed that N-Acetyl-L-aspartic acid and L-Aspartic acid levels mediated the relationship between maternal PPD symptoms and the development of infant problem-solving skills. CONCLUSIONS: Maternal PPD symptoms are associated with alterations in the gut microbiota and neurodevelopment in infants. This study provides new insights into potential early intervention for infants whose mother experienced PPD. Further research is warranted to elucidate the biological mechanisms underlying these associations.
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Towards a psychobiotic therapy for depression: Bifidobacterium breve CCFM1025 reverses chronic stress-induced depressive symptoms and gut microbial abnormalities in mice.
BACKGROUND: Accumulating evidence points to an association between gut microbial abnormalities and depression disorder. The microbiota-gut-brain axis is an emerging target for treating depression using nutritional strategies, considering the numerous limitations of current pharmacological approaches. Here we studied the effect and probable mechanisms of psychobiotic treatment on depression. METHODS: Chronically stressed C57BL/6J male mice were administered viable Bifidobacterium breve CCFM1025 for 5 weeks prior to behavioral testing. Brain neurological alterations, serum corticosterone, cytokines levels, fecal microbial composition, and short-chain fatty acid (SCFA) content were measured. In addition, the effect of SCFA on 5-hydroxytryptophan (5-HTP) biosynthesis was investigated in an in vitro model of enterochromaffin cells (RIN14B). RESULTS: CCFM1025 treatment significantly reduced depression- and anxiety-like behaviors. The hyperactive hypothalamic-pituitary-adrenal response, as well as inflammation, were also alleviated, possibly via regulating the expression of glucocorticoid receptors (Nr3c1). Moreover, CCFM1025 also down-regulated the pCREB-c-Fos pathway but increased the expression of brain-derived neurotrophic factor (BDNF). Meanwhile, chronic stress-induced gut microbial abnormalities were restored, accompanied by increased SCFA and 5-HTP levels. The intestinal 5-HTP biosynthesis positively correlated with fecal SCFA and Bifidobacterium breve levels. CONCLUSIONS: In summary, Bifidobacterium breve CCFM1025 showed considerable antidepressant-like and microbiota-regulating effects, which opens avenues for novel therapeutic strategies towards treating depression.
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Sleep and the gut microbiome in psoriasis: clinical implications for disease progression and the development of cardiometabolic comorbidities.
BACKGROUND: Sleep dysfunction and sleep disorders are important comorbidities of psoriasis. Not only do these sleep comorbidities contribute to reduced quality of life, but they may also lead to worsening psoriasis and increased susceptibility to cardiometabolic diseases. While psoriasis and sleep dysfunction are thought to be linked by itch, depression, and immune system dysregulation, the relationship between psoriasis and sleep dysfunction is not yet fully understood. OBJECTIVE: We sought to compare previous studies characterizing the gut microbiome in psoriasis and sleep dysfunction and examine the potential relevance of shared findings on cardiometabolic and overall health. METHODS: We performed literature searches of PubMed and Embase databases to find studies evaluating the gut microbiome in psoriasis, sleep dysfunction, and cardiometabolic diseases. RESULTS: Studies characterizing the gut microbiome in psoriasis and sleep dysfunction reveal shared findings, specifically an increased Firmicutes to Bacteroidetes ratio and reduced abundance of short chain fatty acid-producing bacteria. These dysbiotic features have also been shown to promote systemic inflammation and cardiometabolic disease. CONCLUSION: In favoring an increased Firmicutes to Bacteroidetes ratio and reduced abundance of short chain fatty acid-producing bacteria, sleep dysfunction could be contributing to worsening psoriasis and cardiometabolic comorbidities through intestinal dysbiosis. Future studies are needed to determine whether gut- and sleep-targeting interventions could be therapeutic in psoriasis patients with poor sleep.
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Probiotics as a Complementary Medicine in Neurologic Disorders.
BACKGROUND AND AIMS: Today, neurological and neuropsychiatric disorders, including depression, anxiety, Parkinson's disease (PD), Alzheimer's disease (AS), autism spectrum disorder (ASD), and multiple sclerosis (MS), contribute significantly to global disability and healthcare burden. Most current treatment options only provide symptomatic relief and are limited by challenges such as drug resistance, systemic side effects, and poor blood-brain barrier permeability. The growing interest in the gut-brain axis has encouraged exploration of the gut microbiota as a potential therapeutic target. Probiotics-live microorganisms that may confer health benefits to the host-have been proposed to modulate the gut-brain axis through immune, metabolic, and neurochemical pathways. METHODS: In this narrative review, a targeted search was performed across multiple databases to identify relevant articles, from which the key relationships and strategies were extracted. Then, we represented the findings to provide a comprehensive overview of the topic and highlight emerging trends and gaps in the literature. RESULTS: Emerging preclinical and clinical studies suggest that specific probiotic strains can improve neurological symptoms by reducing neuroinflammation, supporting gut barrier integrity, and influencing neurotransmitter production. However, findings remain heterogeneous due to strain specificity, individual microbiome diversity, and methodological differences across studies. Preclinical and clinical studies suggest that specific probiotic strains can improve neurological symptoms by reducing neuroinflammation, enhancing gut barrier integrity, and influencing neurotransmitter production. Evidence supports their potential as adjunctive treatments for major neurological and neuropsychiatric disorders, including depression, anxiety, ASD, PD, AD, and MS, particularly in patients with gut dysbiosis or gastrointestinal comorbidities. However, findings remain heterogeneous due to strain specificity, individual microbiome variability, and methodological differences across studies. CONCLUSION: This brief review summarizes the current evidence on the use of probiotics in neurological disorders, discusses potential mechanisms of action, and highlights safety considerations and limitations. Future directions include personalized probiotic therapies, large-scale randomized controlled trials, and integration with conventional neurological therapies. Overall, probiotics could be a low-risk, complementary option in the evolving field of neurotherapy, but more rigorous evidence is needed before definitive clinical recommendations can be made.
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Nutrition and the gut microbiome: a symbiotic dialogue influencing health and disease.
The gut microbiome, a complex consortium of trillions of microorganisms, significantly influences human health through its metabolic activities, immune modulation, and interaction with the nervous system. Diet plays a significant role in shaping the gut microbiome, with plant-based diets promoting the colonization of beneficial bacteria and fiber fermentation, whereas meat-based diet may encourage harmful microbial shifts associated with systemic inflammation. Gut bacteria produce short-chain fatty acids (SCFAs) from dietary fibers and those are crucial for energy metabolism, intestinal integrity, and immune modulation. Certain neurotransmitters like GABA and serotonin produced by gut bacteria, play a vital role in the gut-brain axis. Dysbiosis in the gut microbiota have been linked to various psychiatric and neurological disorders like anxiety, depression, bipolar disorder, Schizophrenia, Alzheimer's and Parkinson's. Beyond neurological implications, the gut microbiota also linked to metabolic and cardiovascular diseases, including obesity, hypertension, and coronary artery disease, as well as colorectal cancer. Imbalances in bacterial ratios, such as Firmicutes to Bacteroidetes, can impact metabolism and inflammation. This review (i) elucidates the complex interplay between nutrition and the gut microbiome, emphasizing its implications for human health and disease; (ii) critically examines the methodological and analytical limitations inherent in current metagenomic studies; and (iii) proposes an integrated, multi-layered, systems-level framework for developing predictive models of host-microbe interactions and their pathological significance.
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Is the Use of Glyphosate in Modern Agriculture Resulting in Increased Neuropsychiatric Conditions Through Modulation of the Gut-brain-microbiome Axis?
Environmental exposure to glyphosate and glyphosate-based herbicides has the potential to negatively influence neurodevelopment and behavior across generations indirectly through the gut-brain-microbiome axis. Potential mechanisms by which glyphosate may elicit these effects are through the disruption of the normally symbiotic relationship of the host and the gut microbiome. Given glyphosate can kill commensal members of the microbiome like Lactobacillus spp., Ruminococaeae and Butyricoccus spp., resulting in reductions in key microbial metabolites that act through the gut-brain-microbiome axis including indoles, L-glutamate and SCFAs. Glyphosate- resistant microbes in the gut have the potential to increase the production of pro-inflammatory cytokines and reactive oxygen species which may result in increased HPA activation, resulting in increased production of glucocorticoids which have implications on neurodevelopment. In addition, maternal transfer of the gut microbiome can affect immune and neurodevelopment, across generations. This perspective article weighs the evidence for chronic glyphosate exposure on the gut microbiome and the potential consequences on the gut-brain axis correlated with increased incidence of neuropsychiatric conditions.
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Epigenetics in depression and gut-brain axis: A molecular crosstalk.
Gut-brain axis is a dynamic, complex, and bidirectional communication network between the gut and brain. Changes in the microbiota-gut-brain axis are responsible for developing various metabolic, neurodegenerative, and neuropsychiatric disorders. According to clinical and preclinical findings, the gut microbiota is a significant regulator of the gut-brain axis. In addition to interacting with intestinal cells and the enteric nervous system, it has been discovered that microbes in the gut can modify the central nervous system through metabolic and neuroendocrine pathways. The metabolites of the gut microbiome can modulate a number of diseases by inducing epigenetic alteration through DNA methylation, histone modification, and non-coding RNA-associated gene silencing. Short-chain fatty acids, especially butyrate, are well-known histone deacetylases inhibitors. Similarly, other microbial metabolites such as folate, choline, and trimethylamine-N-oxide also regulate epigenetics mechanisms. Furthermore, various studies have revealed the potential role of microbiome dysbiosis and epigenetics in the pathophysiology of depression. Hence, in this review, we have highlighted the role of gut dysbiosis in epigenetic regulation, causal interaction between host epigenetic modification and the gut microbiome in depression and suggest microbiome and epigenome as a possible target for diagnosis, prevention, and treatment of depression.
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The Microbiome-Gut-Brain Axis and Resilience to Developing Anxiety or Depression under Stress.
Episodes of depression and anxiety commonly follow the experience of stress, however not everyone who experiences stress develops a mood disorder. Individuals who are able to experience stress without a negative emotional effect are considered stress resilient. Stress-resilience (and its counterpart stress-susceptibility) are influenced by several psychological and biological factors, including the microbiome-gut-brain axis. Emerging research shows that the gut microbiota can influence mood, and that stress is an important variable in this relationship. Stress alters the gut microbiota and plausibly this could contribute to stress-related changes in mood. Most of the reported research has been conducted using animal models and demonstrates a relationship between gut microbiome and mood. The translational evidence from human clinical studies however is rather limited. In this review we examine the microbiome-gut-brain axis research in relation to stress resilience.
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N-3 PUFA Ameliorates the Gut Microbiota, Bile Acid Profiles, and Neuropsychiatric Behaviours in a Rat Model of Geriatric Depression.
The brain-gut-microbiome (BGM) axis affects host bioinformation. N-3 polyunsaturated fatty acids (PUFAs) alleviate cognitive impairment and depression in older adults. This study investigated altered microbiota-bile acid signalling as a potential mechanism linking fish oil-induced gut changes in microbiota to alleviate psychological symptoms. Sprague Dawley rats were fed a fish oil diet and administered D-galactose combined with chronic unpredictable mild stress (CUMS) to simulate geriatric depression. The cognitive function, psychological symptoms, microbiota compositions, and faecal bile acid profiles of the rats were assessed thereafter. A correlation analysis was conducted to determine whether the fish oil-induced alteration of the rats' microbiota and bile acid profiles affected the rats' behaviour. D-galactose and CUMS resulted in lower concentrations of Firmicutes, significantly altered bile acid profiles, and abnormal neurobehaviours. Fish oil intake alleviated the rats' emotional symptoms and increased the abundance of Bacteroidetes, Prevotellaceae, Marinifilaceae, and Bacteroidesuniformis. It also elevated the concentrations of primary bile acids and taurine-conjugated bile acids in the rats' faeces. The rats' taurine-conjugated bile acid levels were significantly correlated with their behavioural outcomes. In short, fish oil intake may alleviate psychological symptoms by altering the microbial metabolites involved in the BGM axis, especially in the conjugation of bile acids.